About this Research Topic
Periodontal disease is a chronic inflammatory condition of the supporting tissues around the teeth, mediated and modulated by the host immune system. Periodontal disease is mainly caused by a dysbiotic biofilm in intimate contact with the gingival tissue, now regarded as the "trigger" of the inflammatory response, that characterizes actively destructive periodontitis. Periodontal disease results in the destruction of surrounding connective tissue (gingiva, periodontal ligament, cement and alveolar bone) ultimately leading to tooth loss if left untreated. The periodontal disease pathophysiology has been well described in its key molecular pathways, and activation of host‐derived proteinases. During the progression of periodontal disease, osteoclasts play a crucial role in the resorption of alveolar bone. Currently, there has been growing interesting in anti-resorptive agents targeting bone loss inhibition during periodontitis progression aiming at diminishing its deleterious effects. Therefore, investigations into the development of new anti-resorptive agents will significantly benefit treatment of periodontal disease.
Osteoclastogenesis, the process essential for the formation of bone-resorbing cells called osteoclasts, is crucial for osteolytic bone pathologies. Thus, pharmacological strategies that target osteoclast differentiation have been used for the treatment of skeletal disorders, such as osteoporosis, rheumatoid arthritis (RA) and periodontitis. Therefore, different classes of osteoclasts inhibitors with varied mechanisms of action were developed. Among them, bisphosphonates, monoclonal antibodies against RANKL, selective estrogen receptor modulators, cathepsins K inhibitors, cystatins C inhibitors and chemically natural compounds, i.e., flavonoids, curcumin, and ginger were also recently described for periodontal disease treatment. Unarguably, numerous studies on the inhibition of osteoclastogenesis during bone metabolic diseases have enabled us to get a greater understanding of host modulation interaction during periodontal disease progression.
In this Research Topic, we welcome manuscripts on bone loss inhibition in periodontitis (translational studies) and other metabolic bone diseases (osteoporosis and RA), their biological effects, host interactions, mechanism(s) of action and consequential inflammatory signaling.
Keywords: Alveolar bone, bisphosphonate, bone, inflammation, osteoclasts, periodontal disease, rheumatoid arthritis
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